Wonderful post on Type B IRS. Insulin Resistance Syndrome. This is an autoimmune disorder, with Antibodies against insulin Receptors which may lead to Dysglycemia like Hypoglycemia or Hyperglycemia. This is associated with severe IR, Acanthosis Nigricans& Hyperandrogenism. This is responsive to immunotherapy. There is a case report where a 55 yr old female with ILD was treated with Steroids and her blood sugar levels went abnormally that she required more than 33,000 Units of insulin a day IV. Still not controlled, then they initiated Prednisone 60 mg TID and the blood sugar levels were maintained for a week and after withdrawal again went back to pavilion. Finally plasmapheresis was done to her. This is an example for Type B IRS. This Syndrome belongs to group of extreme IRS which includes Leprechaunism Rabson Mendenhall Syndrome. Lipodystrophy. This is a rare disorder which occurs in the middle aged adults, predominantly females. The onset of disease usually marked with a rapidly progressive Non ketotic and severely insulin resistance DM along with AN and Hirsutism. Paradoxal hypoglycemia occurs some times. Characteristics of IRS is presence of anti Insulin receptor autoantibodies. Wonderful pictures showing before and after therapy. Classical pictures, thanks Dr Parvez.
absolutely agree with Dr Parvez sir.. these are rare case reports. even I had seen a pt where we have him around 50units/hr iv insulin along with many BOLUS doses of regular insulin around 2500 units per day requirement and still sugars were above 400. unfortunately pt was not satisfied with the treatment as sugars were not coming under control and took discharge and we couldn't follow-up the case.
Hope the below abstract clarify the doubts. Abstract OBJECTIVE: To document a case of type B insulin resistance syndrome associated with systemic lupus erythematosus. METHODS: We present the clinical course of a female patient with type B insulin resistance syndrome, from the onset, diagnosis, and empiric treatment until remission of her disease. RESULTS: A 40-year-old African American woman with systemic lupus erythematosus presented with a relatively acute onset of severe hyperglycemia in January 2004. Her hyperglycemia was resistant to treatment with high doses of insulin (up to an equivalent dose of regular insulin of 4,500 units daily). The diagnosis of type B insulin resistance syndrome was confirmed after her insulin receptor antibody was found to be strongly positive. The patient's hemoglobin Ale level improved substantially after she had been treated with azathioprine for 3 months. By November 2004, she was able to discontinue insulin therapy. Repeated insulin receptor antibody testing in February 2005 revealed that her insulin receptor antibody had become negative. The patient's fasting glucose level became normal, and only occasional mild postprandial hyperglycemic episodes have been noted. CONCLUSION: Immunosuppressive therapy with azathioprine seems to be responsible for our patient's remission of type B insulin resistance, although the possibility of the occurrence of a spontaneous remission cannot be completely excluded.
Dear Prasad, Please come out of insulin shock. Reference is provided for your kind perusal. With regards, Sepuri Krishna Mohan.
Abstract In type B insulin resistance and acanthosis nigricans, the insulin resistance is due to the presence of anti-insulin receptor antibody 1. Approximately one-third of patients with these antibodies have an associated illness such as systemic lupus erythematosus (SLE) or Sjgren's syndrome. This report describes a case wherein the patient had presented with uncontrolled diabetes and required > 3000 units of human insulin to control hyperglycemia. She also had features of SLE. There was complete recovery following treatment with steroids. http://www.ncbi.nlm.nih.gov/pubmed/20374339
Here you go, another case report. A 55 year old African American man with Hepatitis C was treated with interferon and ribavirin. Eight months later he presented with rapid onset of hyperglycemia, profound weakness, and weight loss. Severe hyperglycemia persisted in spite of insulin infusion rates as high as 120 units per hour. Presence of insulin receptorEndocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists Author Manuscript HHS Public Access Type B Insulin Resistance Developing during Interferon Therapy Amanda L. Daniel, M.D., Josetta L. Houlihan, [...], and James P. Walsh, M.D., Ph.D. Additional article information Abstract Objective To report a rare case of diabetes caused by type B insulin resistance due to development of insulin receptor autoantibodies during treatment of hepatitis C with interferon alpha and ribavirin. Methods Clinical and laboratory findings in the case are presented. Literature on type B insulin resistance and interferon-induced autoimmunity is reviewed. Results A 55 year old African American man with Hepatitis C was treated with interferon and ribavirin. Eight months later he presented with rapid onset of hyperglycemia, profound weakness, and weight loss. Severe hyperglycemia persisted in spite of insulin infusion rates as high as 120 units per hour. Presence of insulin receptor autoantibodies was confirmed by immunoprecipitation of recombinant human insulin receptor with patient serum. Assays for autoantibodies to islet cell antigens and glutamic acid decarboxylase were negative. The interferon and ribavirin were discontinued. His insulin requirement spontaneously fell to low levels and his blood glucose measurements normalized over ajournal of the American College of Endocrinology and the American Association of Clinical Endocrinologists Author Manuscript HHS Public Access Type B Insulin Resistance Developing during Interferon Therapy Amanda L. Daniel, M.D., Josetta L. Houlihan, [...], and James P. Walsh, M.D., Ph.D. Additional article information Abstract Objective To report a rare case of diabetes caused by type B insulin resistance due to development of insulin receptor autoantibodies during treatment of hepatitis C with interferon alpha and ribavirin. Methods Clinical and laboratory findings in the case are presented. Literature on type B insulin resistance and interferon-induced autoimmunity is reviewed. Results A 55 year old African American man with Hepatitis C was treated with interferon and ribavirin. Eight months later he presented with rapid onset of hyperglycemia, profound weakness, and weight loss. Severe hyperglycemia persisted in spite of insulin infusion rates as high as 120 units per hour. Presence of insulin receptor autoantibodies was confirmed by immunoprecipitation of recombinant human insulin receptor with patient serum. Assays for autoantibodies to islet cell antigens and glutamic acid decarboxylase were negative. The interferon and ribavirin were discontinued. His insulin requirement spontaneously fell to low levels and his blood glucose measurements normalized over a six month period. Two years later, insulin receptor autoantibodies could no longer be demonstrated in his serum. He remains euglycemic and is no longer taking insulin.
Just to make you wake up little bit more.... Type B insulin resistance is a rare autoimmune disease characterized by the presence of autoantibodiesBMC Endocrine Disorders BioMed Central Type B insulin resistance syndrome with Scleroderma successfully treated with multiple immune suppressants after eradication of Helicobacter pylori infection: a case report Guo-Qing Yang, Yi-Jun Li, [...], and Yi-Ming Mu Additional article information Abstract Background Type B insulin resistance is a rare autoimmune disease characterized by the presence of autoantibodies against the insulin receptor. Helicobacter pylori (H pylori) infection may play a causative role in the autoimmune diseases. Case presentation Here, we present a rare case of a 48-year old female patient, who had type B insulin resistance with systemic scleroderma and was successfully treated with multiple..... s given at high doses, including glymepiride 6mg/day, metformin 2.0g/day, and pioglitazone 30mg/day. Insulin therapy was added, but her blood glucose was higher than 15mmol/L in the daytime despite that doses were up to 18,000 units/day with continuous insulin (including human regular insulin and rapid-acting insulin) infusion. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855773/
I am still on wait for reply from Dr Parvez and Dr Krisna Mohan sirs for my rejoinder to the former's abstra t posted above. I feel it my duty to further straighten the matter under consideratin. The case quoted is not a prospective or retospective study of considerable sample size but is just a reporting of a rare case (case rrport) whose veracity is questionable. The deference between aim and objectives is thin. The Aim is presenting an interesting case of....so and so. where as the author presents the same as objectives (technically used for a studuy).likewise material and methods are irrelevant to the theme of presentation. so is the Reslts part. The conclusion is far reaching in view of sample size (N=1) that spontaneous remission is possible which means accepting that the remession could be spontaneou . Use of a drug other than tegular insuiln and concludibg it'potency interms regular insulin is make believe at the best. Tons of( not glucogon) such papers could b produced in notime and publication of such "stuff" is not difficult in view of price tag by the journals ( Don't mean mediscope) for "Encoiraging" such publications. There is discount for papers coming from underdeveloped countries. It is not difficult to asess the authencity of a paper if such exercise is undertaken atall. The paradox is all published dsta point out unanimously the hypoglycemic effect (except few case reports like the two 33000 and 2400 u) which report as insulin resistance (exact opposite).The reason for the reported hypogycemic effect is postulated as being due to the antibodies to INSULIN RECPTOR BEING COMPLIMENTARY TO INSULIN ENHANCING INSULIN EFFECT (THUS HYPOGLYCEMIC EFFECT) RATHER THAN IR requiring large (elephentine)doses of insulin As such the reports claimg tequirement in tens of thousands is an criminal act which could be fit for legal recourse. it is a foregone concusion that that the clarification would not be appreciated even by a single Curafian and is against Curafy tradition, customs and protocals. A good task done is itself rewardind-a sort of self satisfaction which I had in plenty. so Curafianspl skip this if u have not already done.
sir do u really mean that the pt required 33000 u/ day iv and still did not respond....... if so it is surely a land mark case.
No where in the article it says Insulin X. It says high doses of Insulin up to 4,500 units of Regular Insulin was given. Type B Insulin resistance is a rare disease. You cannot have Prospective RCT on rare disease, except literature review on case report or case series. If you have any references to counter the above article, why don't you provide for discussion, instead of continued to be happy in comatose state ?
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Lupus is a chronic autoimmune disease in which the body’s immune system becomes hyperactive and attacks normal, healthy tissue. This results in symptoms such as inflammation, swelling, and damage to joints, skin, kidneys, blood, the heart, and lungs. Under normal function, the immune system makes proteins called antibodies in order to protect and fight against antigens such as viruses and bacteria. Lupus makes the immune system unable to differentiate between antigens (a substance capable of inducing a specific immune response) and healthy tissue. This leads the immune system to direct antibodies against the healthy tissue – not just antigens – causing swelling, pain, and tissue damage. History The history of lupus can be divided into three periods: classical, neoclassical, and modern. This article concentrates on developments in the present century which have greatly expanded our knowledge about the pathophysiology, clinical-laboratory features, and treatment of this disorder. Lupus in the classical period (1230-1856) The history of lupus during the classical period was reviewed by Smith and Cyr in 1988. Of note are the derivation of the term lupus and the clinical descriptions of the cutaneous lesions of lupus vulgaris, lupus profundus, discoid lupus, and the photosensitive nature of the malar or butterfly rash. The word ‘lupus’ (Latin for ‘wolf’) is attributed to the thirteenth century physician Rogerius who used it to describe erosive facial lesions that were reminiscent of a wolf’s bite. Classical descriptions of the various dermatologic features of lupus were made by Thomas Bateman, a student of the British dermatologist Robert William, in the early nineteenth century; Cazenave, a student of the French dermatologist Laurent Biett, in the mid-nineteenth century; and Moriz Kaposi (born Moriz Kohn), student and son-in-law of the Austrian dermatologist Ferdinand von Hebra, in the late nineteenth century. The lesions now referred to as discoid lupus were described in 1833 by Cazenave under the term “erythema centrifugum,” while the butterfly distribution of the facial rash was noted by von Hebra in 1846. The first published illustrations of lupus erythematosus were included in von Hebra’s text, Atlas of Skin Diseases, published in 1856. Lupus in the neoclassical period (1872- 1948) The Neoclassical era of the history of lupus began in 1872 when Kaposi first described the systemic nature of the disorder: “…experience has shown that lupus erythematosus … may be attended by altogether more severe pathological changes, and even dangerous constitutional symptoms may be intimately associated with the process in question, and that death may result from conditions which must be considered to arise from the local malady.” Kaposi proposed that there were two types of lupus erythematosus; the discoid form and a disseminated (systemic) form. Furthermore, he enumerated various signs and symptoms which characterized the systemic form, including: subcutaneous nodules arthritis with synovial hypertrophy of both small and large joints lymphadenopathy fever weight loss anemia central nervous system involvement The existence of a systemic form of lupus was firmly established in 1904 by the work of Osler in Baltimore and Jadassohn in Vienna. Over the next thirty years, pathologic studies documented the existence of nonbacterial verrucous endocarditis (Libman-Sacks disease) and wire-loop lesions in individuals with glomerulonephritis; such observations at the autopsy table led to the construct of collagen disease proposed by Kemperer and colleagues in 1941. This terminology, ‘collagen vascular disease,’ persists in usage more than seventy years after its introduction. Lupus in the modern era (1948-present) The sentinel event which heralded the modern era was the discovery of the LE cell by Hargraves and colleagues in 1948. The investigators observed these cells in the bone marrow of individuals with acute disseminated lupus erythematosus and postulated that the cell “…is the result of…phagocytosis of free nuclear material with a resulting round vacuole containing this partially digested and lysed nuclear material…”. This discovery ushered in the present era of the application of immunology to the study of lupus erythematosus; it also allowed the diagnosis of individuals with much milder forms of the disease. This possibility, coupled with the discovery of cortisone as a treatment, changed the natural history of lupus as it was known prior to that time. Two other immunologic markers were recognized in the 1950s as being associated with lupus: the biologic false-positive test for syphilis and the immunofluorescent test for antinuclear antibodies. Moore, working in Baltimore, demonstrated that systemic lupus developed in 7 percent of 148 individuals with chronic false-positive tests for syphilis and that a further 30 percent had symptoms consistent with collagen disease. Friou applied the technique of indirect immunofluorescence to demonstrate the presence of antinuclear antibodies in the blood of individuals with systemic lupus. Subsequently, there was the recognition of antibodies to deoxyribonucleic acid (DNA) and the description of antibodies to extractable nuclear antigens (nuclear ribonucleoprotein [nRNP], Sm, Ro, La), and anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and understanding the etiopathogenesis of lupus. The Lupus Erythematosus cell is discovered. This discovery ushered in the present era of the application of immunology to the study of lupus erythematosus; it also allowed the diagnosis of individuals with much milder forms of the disease. This possibility, coupled with the discovery of cortisone as a treatment, changed the natural history of lupus as it was known prior to that time. Two other immunologic markers were recognized in the 1950s as being associated with lupus: the biologic false-positive test for syphilis and the immunofluorescent test for antinuclear antibodies. Moore, working in Baltimore, demonstrated that systemic lupus developed in 7 percent of 148 individuals with chronic false-positive tests for syphilis and that a further 30 percent had symptoms consistent with collagen disease. Friou applied the technique of indirect immunofluorescence to demonstrate the presence of antinuclear antibodies in the blood of individuals with systemic lupus. Subsequently, there was the recognition of antibodies to deoxyribonucleic acid (DNA) and the description of antibodies to extractable nuclear antigens (nuclear ribonucleoprotein [nRNP], Sm, Ro, La), and anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and understanding the etiopathogenesis of lupus. Genetic component recognized The familial occurrence of systemic lupus was first noted by Leonhardt in 1954 and later studies by Arnett and Shulman at Johns Hopkins. Subsequently, familial aggregation of lupus, the concordance of lupus in monozygotic twin pairs, and the association of genetic markers with lupus have been described over the past twenty years. Molecular biology techniques have been applied to the study of human lymphocyte antigen (HLA) Class II genes to determine specific amino acid sequences in these cell surface molecules that are involved in antigen presentation to T-helper cells in individuals with lupus. These studies have resulted in the identification of genetic-serologic subsets of systemic lupus that complement the clinico-serologic subsets noted earlier. It is hoped by investigators working in this field that these studies will lead to the identification of etiologic factors (e.g., viral antigens/proteins) in lupus. Over the last decade or so, we have witnessed significant advances in the understanding of the genetic basis of lupus, and of the immunological derangements which lead to the clinical manifestations of the disease. Advances have been made in the assessment of the impact of the disease in general, and in minority population groups, in particular and efforts are being made towards defining lupus biomarkers which may help both to predict disease outcome and to guide treatments. Prevalence and incidence Lupus appears to be a relatively uncommon disease. The prevalence has been estimated in several different countries mostly, however, in the developed world, using different techniques of case ascertainment. The authors of one metaanalysis (including those studies in Europe and North America) suggested an overall weighted mean prevalence of 24/100,000 population.Three English studies have produced prevalence estimates of: 12/100,000, 25/100,000 and 28/100,000 and the only study in N Ireland estimated a rate of 254/100,000. Studies in countries which include predominantly white populations have resulted in lower prevalence estimates (e.g. England) when compared with studies among populations with a significant proportion of Afro-Caribbeans, Asians and Hispanics. It is more difficult to estimate incidence for a rare disease but studies in both North America and Europe have produced estimates that are similar (approximately 1 – 8 cases per 100,000 persons per year).The lowest rates of incidence were seen among Caucasian Americans, Canadians and Spaniards and the highest rates among Asian (10.0 cases /100,000) and Afro-Caribbean (21.9 cases /100,000) residents of the UK. In an average UK practice list of 3000 patients, therefore, a GP would not expect to see a new case of lupus more often than every 7-10 years. Types There are three main types of lupus: Systemic lupus erythematosus (eh-RITH-eh-muh-TOE-sus) is the most common form. It’s sometimes called SLE, or just lupus. The word “systemic” means that the disease can involve many parts of the body such as the heart, lungs, kidneys, and brain. SLE symptoms can be mild or serious. Systemic lupus Discoid lupus erythematosus mainly affects the skin. A red rash may appear, or the skin on the face, scalp, or elsewhere may change color. Discoid lupus Drug-induced lupus is triggered by a few medicines. It’s like SLE, but symptoms are usually milder. Most of the time, the disease goes away when the medicine is stopped. More men develop drug-induced lupus because the drugs that cause it, hydralazine and procainamide, are used to treat heart conditions that are more common in men. Risk factors Risk factors for developing lupus include: Gender – more than 90% of people with lupus are women. Before puberty, boys and girls are equally likely to develop the condition Age – symptoms and diagnosis of lupus often occur between the ages of 15-45. Around 15% of people who are later diagnosed with lupus, experienced symptoms before the age of 18 Race – in the US, lupus is more common, more severe and develops earlier in African-Americans, Hispanics/Latinos, Asian-Americans, Native Americans, Native Hawaiians and Pacific Islanders than in the white population Family history – first-degree or second-degree relatives of a person with lupus have a 4-8% risk of developing lupus. One study suggests that sisters of lupus patients have as high as a 10% chance of developing lupus. In another 10-year prospective study, researchers observed a 7% incidence of lupus in first-degree relatives of lupus patients. Causes Many (but not all) scientists believe that lupus develops in response to a combination of factors both inside and outside the body, including hormones, genetics, and environment. Hormones Hormones are the body’s messengers. They regulate many of the body’s functions. Because nine of every 10 occurrences of lupus are in females, researchers have looked at the relationship between estrogen and lupus. While men and women both produce estrogen, its production is much greater in females. Many women have more lupus symptoms before menstrual periods and/or during pregnancy when estrogen production is high. This may indicate that estrogen somehow regulates the severity of lupus. However, no causal effect has been proven between estrogen, or any other hormone, and lupus. And, studies of women with lupus taking estrogen in either birth control pills or as postmenopausal therapy have shown no increase in significant disease activity. Researchers are now focusing on differences between men and women, beyond hormone levels, which may account for why women are more prone to lupus and other autoimmune diseases. Genetics Researchers have now identified more than 50 genes which they associate with lupus. These genes are more commonly seen in people with lupus than in those without the disease, and while most of these genes have not been shown to directly cause lupus, they are believed to contribute to it. In most cases, genes are not enough. This is especially evident with twins who are raised in the same environment and have the same inherited features yet only one develops lupus. Although, when one of two identical twins has lupus, there is an increased chance that the other twin will also develop the disease (30% percent chance for identical twins; 5-10% percent chance for fraternal twins). Lupus can develop in people with no family history of it, but there are likely to be other autoimmune diseases in some family members. Certain ethnic groups (people of African, Asian, Hispanic/Latino, Native American, Native Hawaiian, or Pacific Island descent) have a greater risk of developing lupus, which may be related to genes they have in common. Environment Most researchers today think that an environmental agent, such as a virus or possibly a chemical, randomly encountered by a genetically susceptible individual, acts to trigger the disease. Researchers have not identified a specific environmental agent as yet but the hypothesis remains likely. While the environmental elements that can trigger lupus and cause flares aren’t fully known, the most commonly cited are ultraviolet light (UVA and UVB); infections (including the effects of the Epstein-Barr virus), and exposure to silica dust in agricultural or industrial settings. Symptoms Lupus can have many symptoms, and they differ from person to person. Some of the more common ones are Pain or swelling in joints Muscle pain Fever with no known cause Red rashes, most often on the face (also called the “butterfly rash”) Chest pain when taking a deep breath Hair loss Pale or purple fingers or toes Sensitivity to the sun Swelling in legs or around eyes Mouth ulcers Swollen glands Feeling very tired Symptoms may come and go. When you are having symptoms, it is called a flare. Flares can range from mild to severe. New symptoms may appear at any time. Diagnosis and test Diagnosing lupus is difficult because signs and symptoms vary considerably from person to person. Signs and symptoms of lupus may vary over time and overlap with those of many other disorders. No one test can diagnose lupus. The combination of blood and urine tests, signs and symptoms, and physical examination findings leads to the diagnosis. Laboratory tests Blood and urine tests may include: Complete blood count: This test measures the number of red blood cells, white blood cells and platelets as well as the amount of hemoglobin, a protein in red blood cells. Results may indicate you have anemia, which commonly occurs in lupus. A low white blood cell or platelet count may occur in lupus as well. Erythrocyte sedimentation rate: This blood test determines the rate at which red blood cells settle to the bottom of a tube in an hour. A faster than normal rate may indicate a systemic disease, such as lupus. The sedimentation rate isn’t specific for any one disease. It may be elevated if you have lupus, another inflammatory condition, cancer or an infection. Kidney and liver assessment: Blood tests can assess how well your kidneys and liver are functioning. Lupus can affect these organs. Urinalysis. An examination of a sample of your urine may show an increased protein level or red blood cells in the urine, which may occur if lupus has affected your kidneys. Antinuclear antibody (ANA) test. A positive test for the presence of these antibodies — produced by your immune system — indicates a stimulated immune system. While most people with lupus have a positive ANA test, most people with a positive ANA do not have lupus. If you test positive for ANA, your doctor may advise more-specific antibody testing. Imaging tests If your doctor suspects that lupus is affecting your lungs or heart, he or she may suggest: Chest X-ray. An image of your chest may reveal abnormal shadows that suggest fluid or inflammation in your lungs. Echocardiogram. This test uses sound waves to produce real-time images of your beating heart. It can check for problems with your valves and other portions of your heart. Biopsy Lupus can harm your kidneys in many different ways, and treatments can vary, depending on the type of damage that occurs. In some cases, it’s necessary to test a small sample of kidney tissue to determine what the best treatment might be. The sample can be obtained with a needle or through a small incision. Treatment and medications Treatment for lupus depends on your signs and symptoms. Determining whether your signs and symptoms should be treated and what medications to use requires a careful discussion of the benefits and risks with your doctor. As your signs and symptoms flare and subside, you and your doctor may find that you’ll need to change medications or dosages. The medications most commonly used to control lupus include: Nonsteroidal anti-inflammatory drugs (NSAIDs): Over-the-counter NSAIDs, such as naproxen sodium (Aleve) and ibuprofen (Advil, Motrin IB, others), may be used to treat pain, swelling and fever associated with lupus. Stronger NSAIDs are available by prescription. Side effects of NSAIDs include stomach bleeding, kidney problems and an increased risk of heart problems. Antimalarial drugs: Medications commonly used to treat malaria, such as hydroxychloroquine (Plaquenil), also can help control lupus. Side effects can include stomach upset and, very rarely, damage to the retina of the eye. Corticosteroids: Prednisone and other types of corticosteroids can counter the inflammation of lupus but often produce long-term side effects including weight gain, easy bruising, thinning bones (osteoporosis), high blood pressure, diabetes and increased risk of infection. The risk of side effects increases with higher doses and longer term therapy. Immunosuppressants: Drugs that suppress the immune system may be helpful in serious cases of lupus. Examples include azathioprine (Imuran, Azasan), mycophenolate (CellCept), leflunomide (Arava) and methotrexate (Trexall). Potential side effects may include an increased risk of infection, liver damage, decreased fertility and an increased risk of cancer. A newer medication, belimumab (Benlysta), also reduces lupus symptoms in some people. Side effects include nausea, diarrhea and fever. Prevention There is no known way to prevent Lupus since there is no known cause as yet. You can help manage flare-ups though: Avoid known triggers such as sunlight, stress, and lack of sleep Manage your diet Get adequate exerciseDr. Nitin Kanholkar1 Like7 Answers
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Autoimmune Diseases: Types, Symptoms, Causes and More........Check it Out...! ---------------------------------------------------------------------- ---------------------------------------------------------------------- What is an autoimmune disease? An autoimmune disease is a condition in which your immune system mistakenly attacks your body. The immune system normally guards against germs like bacteria and viruses. When it senses these foreign invaders, it sends out an army of fighter cells to attack them. Normally, the immune system can tell the difference between foreign cells and your own cells. In an autoimmune disease, the immune system mistakes part of your body — like your joints or skin — as foreign. It releases proteins called autoantibodies that attack healthy cells. Some autoimmune diseases target only one organ. Type 1 diabetes damages the pancreas. Other diseases, like lupus, affect the whole body. CAUSES Why does the immune system attack the body? Doctors don’t know what causes the immune system misfire. Yet some people are more likely to get an autoimmune disease than others. Women get autoimmune diseases at a rate of about 2 to 1 compared to men — 6.4 percent of women vs. 2.7 percent of men . Often the disease starts during a woman’s childbearing years (ages 14 to 44). Some autoimmune diseases are more common in certain ethnic groups. For example, lupus affects more African-American and Hispanic people than Caucasians. Certain autoimmune diseases, like multiple sclerosis and lupus, run in families. Not every family member will necessarily have the same disease, but they inherit a susceptibility to an autoimmune condition. Because the incidence of autoimmune diseases is rising, researchers suspect environmental factors like infections and exposures to chemicals or solvents might also be involved . A “Western” diet is another suspected trigger. Eating high-fat, high-sugar, and highly processed foods is linked to inflammation, which might set off an immune response. However, this hasn’t been proven . Another theory is called the hygiene hypothesis. Because of vaccines and antiseptics, children today aren’t exposed to as many germs as they were in the past. The lack of exposure could make their immune system overreact to harmless substances . BOTTOM LINE: Researchers don’t know exactly what causes autoimmune diseases. Diet, infections, and exposure to chemicals might be involved. COMMON AUTOIMMUNE DISEASES 14 common autoimmune diseases There are more than 80 different autoimmune diseases . Here are 14 of the most common ones. 1. Type 1 diabetes The pancreas produces the hormone insulin, which helps regulate blood sugar levels. In type 1 diabetes, the immune system attacks and destroys insulin-producing cells in the pancreas. High blood sugar can damage blood vessels, as well as organs like the heart, kidneys, eyes, and nerves. 2. Rheumatoid arthritis (RA) In rheumatoid arthritis (RA), the immune system attacks the joints. This attack causes redness, warmth, soreness, and stiffness in the joints. Unlike osteoarthritis, which affects people as they get older, RA can start as early as your 30s . 3. Psoriasis/psoriatic arthritis Skin cells normally grow and then shed when they’re no longer needed. Psoriasis causes skin cells to multiply too quickly. The extra cells build up and form red, scaly patches called scales or plaques on the skin. About 30 percent of people with psoriasis also develop swelling, stiffness, and pain in their joints . This form of the disease is called psoriatic arthritis. 4. Multiple sclerosis Multiple sclerosis (MS) damages the myelin sheath — the protective coating that surrounds nerve cells. Damage to the myelin sheath affects the transmission of messages between your brain and body. This damage can lead to symptoms like numbness, weakness, balance issues, and trouble walking. The disease comes in several forms, which progress at different rates. About 50 percent of people with MS need help walking within 15 years after getting the disease. 5. Systemic lupus erythematosus (lupus) Although doctors in the 1800s first described lupus as a skin disease because of the rash it produces, it actually affects many organs, including the joints, kidneys, brain, and heart . Joint pain, fatigue, and rashes are among the most common symptoms. 6. Inflammatory bowel disease Inflammatory bowel disease (IBD) is a term used to describe conditions that cause inflammation in the lining of the intestines. Each type of IBD affects a different part of the GI tract. Crohn’s disease can inflame any part of the GI tract, from the mouth to the anus. Ulcerative colitis affects only the lining of the large intestine (colon) and rectum. 7. Addison’s disease Addison’s disease affects the adrenal glands, which produce the hormones cortisol and aldosterone. Having too little of these hormones can affect the way the body uses and stores carbohydrates and sugar. Symptoms include weakness, fatigue, weight loss, and low blood sugar. 8. Graves’ disease Graves’ disease attacks the thyroid gland in the neck, causing it to produce too much of its hormones. Thyroid hormones control the body’s energy usage, or metabolism. Having too much of these hormones revs up your body’s activities, causing symptoms like nervousness, a fast heartbeat, heat intolerance, and weight loss. One common symptom of this disease is bulging eyes, called exophthalmos. It affects up to 50 percent of people with Graves’ disease . 9. Sjögren’s syndrome This condition attacks the joints, as well as glands that provide lubrication to the eyes and mouth. The hallmark symptoms of Sjögren’s syndrome are joint pain, dry eyes, and dry mouth. 10. Hashimoto’s thyroiditis In Hashimoto’s thyroiditis, thyroid hormone production slows. Symptoms include weight gain, sensitivity to cold, fatigue, hair loss, and swelling of the thyroid (goiter). 11. Myasthenia gravis Myasthenia gravis affects nerves that help the brain control the muscles. When these nerves are impaired, signals can’t direct the muscles to move. The most common symptom is muscle weakness that gets worse with activity and improves with rest. Often muscles that control swallowing and facial movements are involved. 12. Vasculitis Vasculitis happens when the immune system attacks blood vessels. The inflammation that results narrows the arteries and veins, allowing less blood to flow through them. 13. Pernicious anemia This condition affects a protein called intrinsic factor that helps the intestines absorb vitamin B-12 from food. Without this vitamin, the body can’t make enough red blood cells. Pernicious anemia is more common in older adults. It affects 0.1 percent of people in general, but nearly 2 percent of people over age 60 . 14. Celiac disease People with celiac disease can’t eat foods containing gluten — a protein found in wheat, rye, and other grain products. When gluten is in the intestine, the immune system attacks it and causes inflammation. Celiac disease affects about 1 percent of people in the United States . A larger number of people have gluten sensitivity, which isn’t an autoimmune disease, but can have similar symptoms like diarrhea and abdominal pain. SYMPTOMS Autoimmune disease symptoms The early symptoms of many autoimmune diseases are very similar, such as: fatigue achy muscles swelling and redness low-grade fever trouble concentrating numbness and tingling in the hands and feet hair loss skin rashes Individual diseases can also have their own unique symptoms. For example, type 1 diabetes causes extreme thirst, weight loss, and fatigue. IBD causes belly pain, bloating, and diarrhea. With autoimmune diseases like psoriasis or RA, symptoms come and go. Periods of symptoms are called flare-ups. Periods when the symptoms go away are called remissions. BOTTOM LINE: Symptoms like fatigue, muscle aches, swelling, and redness could be signs of an autoimmune disease. Often symptoms come and go over time. SEE A DOCTOR When to see a doctor See a doctor if you have symptoms of an autoimmune disease. You might need to visit a specialist, depending on the type of disease you have. Rheumatologists treat joint diseases like rheumatoid arthritis and Sjögren’s syndrome. Gastroenterologists treat diseases of the GI tract, such as celiac and Crohn’s disease. Endocrinologists treat conditions of the glands, including Graves’ and Addison’s disease. Dermatologists treat skin conditions such as psoriasis. DIAGNOSIS Tests that diagnose autoimmune diseases No single test can diagnose most autoimmune diseases. Your doctor will use a combination of tests and an assessment of your symptoms to diagnose you. The antinuclear antibody test (ANA) is often the first test that doctors use when symptoms suggest an autoimmune disease. A positive test means you likely have one of these diseases, but it won’t confirm exactly which one you have. Other tests look for specific autoantibodies produced in certain autoimmune diseases. Your doctor might also do tests to check for the inflammation these diseases produce in the body. BOTTOM LINE: A positive ANA blood test can show that you have an autoimmune disease. Your doctor can use your symptoms and other tests to confirm the diagnosis. TREATMENT How are autoimmune diseases treated? Treatments can’t cure autoimmune diseases, but they can control the overactive immune response and bring down inflammation. Drugs used to treat these conditions include: nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin, Advil) and naproxen (Naprosyn) immune-suppressing drugs Treatments are also available to relieve symptoms like pain, swelling, fatigue, and skin rashes. Eating a well-balanced diet and getting regular exercise can also help you feel better. BOTTOM LINE: The main treatment for autoimmune diseases is with medications that bring down inflammation and calm the overactive immune response. Treatments can also help relieve symptoms. BOTTOM LINE The bottom line More than 80 different autoimmune diseases exist. Often their symptoms overlap, making them hard to diagnose. Autoimmune diseases are more common in women, and they often run in families. Blood tests that look for autoantibodies can help doctors diagnose these conditions. Treatments include medicines to calm the overactive immune response and bring down inflammation in the body.Dr. V Srivastava7 Likes7 Answers
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45 yr Female with chest pain on/off 3 months associated with cough . Generalized body pains +, Joint pains + Her chest x ray and CECT chest done. Autoimmune profile done. Reports attached. @Sandeep GhodekarDr. Neeraj Mumwalia0 Like4 Answers
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WHAT IS MPGN Membranoproliferative glomerulonephritis (MPGN) is a disease that affects the glomeruli, or filters, of the kidneys. Most instances of MPGN are caused by other diseases or disorders, including autoimmune diseases (such as systemic lupus erythematosis), chronic infections (like hepatitis B or more commonly hepatitis C), monoclonal immunoglobulin deposition diseases, and hereditary diseases. However, a few cases are idiopathic, or of unknown cause. The idiopathic type of MPGN is seen more commonly in persons aged 8-40 MICROSCOPIC TYPES There are three histologic (microscopic) types of MPGN, each of which has a different appearance under the microscope. Type I– Discrete immune complexes are found in the mesangium and subendothelial space. Immune complexes are combinations of antigens and antibodies which bind to each other and then become lodged in the kidney. This activates the immune system, which causes inflammation and damage to the kidney itself. Type II – This is also called dense deposit disease. When viewed under the microscope, continuous, dense ribbon-like deposits are found along the basement membranes of the glomeruli, tubules, and Bowman’s capsule. Type III – This is also an immune complex disease, similar to Type I. However, the immune complexes are found in the subepithelial space, and there is disruption of the glomerular basement membrane with large open areas. What are the symptoms? The symptoms of MPGN are very similar to those of a focal glomerulonephritis. Specifically, patients have hematuria (blood in the urine), either macroscopic, which can be seen by the naked eye, or microscopic. Many of the red blood cells are dysmorphic (malformed or misshapen). In addition, mild or severe proteinuria can be found (including the nephrotic syndrome). What is the treatment? When MPGN is associated with another condition or disease, it is usually resolved by successfully treating the associated condition or disease. However, the optimal treatment of idiopathic MPGN is not entirely known. The type of treatment will depend on the type of proteinuria that the patient has. If a patient has proteinuria that is “non-nephrotic”, then specific immunosuppressive therapy may not be necessary, as the long-term outcome is not life-threatening. However, patients with nephrotic-range proteinuria will typically be treated with steroids (Prednisone).Sushmita Haodijam2 Likes1 Answer
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35 years old female suffering from recurrent painless nonitchy swelling for last 5 years. No h/o respiratory distress. No family history of such lesions. She is a known Hypertensive and for that she is on Telmisertan 40 mg/day. Patient has been treated with Levocetirizine 10mg twice a day for six months and Monteleukast 10 mg at night for six months, but no relief. Only responding to short courses of systematic Steroid 2 mg /kg with tapering dose. 1). Diagnosis 2). D/D 3). Investigations 4). Management. Please give your answers in chronological order.Dr. Sankar Kumar Das10 Likes19 Answers